miR-187 modulates cardiomyocyte apoptosis and oxidative stress in myocardial infarction mice via negatively regulating DYRK2

Myocardial infarction is a serious representation of cardiovescular disease, MicroRNAs play role in modifying I/R injury and myocardial infarct remodeling. The present study therefore examined the potential miR-187 cardiac its underlying mechanisms. was inhibited or overexpressed cardiomyocytes H/R models by pretreatment with mimic inhibitor to confirm function H/R. DYRK2 inhibitor. A myocardium mouse model established. Circulating levels detected quantitative realtime PCR protein expression western blotting. cell viability all groups determined MTT assay apoptosis ratio flow cytometry after staining Annexin V-FITC. effect on cellular ROS generation DCFH-DA. level lipid peroxidation SOD were MDA assay. findings indicated that may be possible regulator protective H/R-induced cardiomyocyte apoptosis, oxidative stress leaded suppression at posttranscriptional level. Moreover, improvement contributed obstruction expression. In addition, these results identified as functional downstream target regulated stress.These work provided first insight into successfully protect both vivo vitro, such mediated through regulation